Voacangine, a naturally occurring alkaloid, has been testified to display beneficial effects on a variety of human diseases, but its role in ischemic stroke is unclear. The impacts of voacangine on oxygen–glucose deprivation/reoxygenation (OGD/R)‐tempted hippocampal neuronal cells are investigated. The bioinformatics analysis found that voacangine is a bioactive ingredient that may have good effects on ischemic stroke. KEGG pathways analysis found that voacangine may regulate ischemic stroke through modulating the PI3K‐Akt‐FoxO signaling pathway. Voacangine could mitigate OGD/R‐tempted cytotoxicity in HT22 cells. Voacangine mitigated OGD/R‐tempted oxidative stress in HT22 cells by diminishing reactive oxygen species level and enhancing superoxide dismutase level. Voacangine mitigated OGD/R‐tempted ferroptosis in HT22 cells. Voacangine promoted activation of the PI3K‐Akt‐FoxO signaling in OGD/R‐induced HT22 cells. Inactivation of the PI3K‐Akt‐FoxO signaling pathway reversed the protective effects of voacangine against OGD/R‐tempted oxidative stress, cytotoxicity, and ferroptosis in HT22 cells. In conclusion, voacangine protects hippocampal neuronal cells against OGD/R‐caused oxidative stress and ferroptosis by activating the PI3K‐Akt‐FoxO signaling.

中文翻译：

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Voacangine 通过激活 PI3K-Akt-FoxO 信号传导保护海马神经元细胞免受氧-葡萄糖剥夺/再氧合引起的氧化应激和铁死亡


Voacangine 是一种天然存在的生物碱，已被证明对多种人类疾病有益，但其在缺血性中风中的作用尚不清楚。研究了 voacangine 对氧-葡萄糖剥夺/再氧合 （OGD/R） 诱惑的海马神经元细胞的影响。生物信息学分析发现，voacangine 是一种生物活性成分，可能对缺血性中风有很好的效果。KEGG 通路分析发现，voacangine 可能通过调节 PI3K‐Akt‐FoxO 信号通路来调节缺血性脑卒中。Voacangine 可以减轻 HT22 细胞中 OGD/R 诱发的细胞毒性。Voacangine 通过降低活性氧水平和提高超氧化物歧化酶水平来减轻 HT22 细胞中 OGD/R 诱发的氧化应激。Voacangine 减轻 HT22 细胞中 OGD/R 诱发的铁死亡。Voacangine 促进 OGD/R 诱导的 HT22 细胞中 PI3K‐Akt‐FoxO 信号转导的激活。PI3K-Akt-FoxO 信号通路的失活逆转了 voacangine 对 HT22 细胞中 OGD/R 诱发的氧化应激、细胞毒性和铁死亡的保护作用。总之，voacangine 通过激活 PI3K-Akt-FoxO 信号传导保护海马神经元细胞免受 OGD/R 引起的氧化应激和铁死亡。